Secondary and Tertiary Hyperparathyroidism — MCQs
Bones, stones, abdominal groans, and psychiatric overtones are features of?
Which of the following is not a treatment option for hypercalcemia?
A 10-year-old boy has a fracture of the femur. Biochemical evaluation revealed a hemoglobin level of 11.5 g/dL and an erythrocyte sedimentation rate of 18 mm in the first hour. Serum calcium levels were 12.8 mg/dL, serum phosphorus levels were 2.3 mg/dL, alkaline phosphatase levels were 28 KA units, and blood urea levels were 32 mg/dL. Which of the following is the most probable diagnosis in his case?
What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?
All are true about primary hyperparathyroidism except which of the following?
A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?
A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -
False about syphilis is :
A 20-year-old male presents to the emergency department with a head injury. Examination reveals normal consciousness, no neurological deficits, and blood in the tympanic membrane. What is the most likely cause?
Where is a bruit typically heard in the thyroid gland?
Secondary and Tertiary Hyperparathyroidism Indian Medical PG Practice Questions and MCQs
Question 1: Bones, stones, abdominal groans, and psychiatric overtones are features of?
- A. Hypothyroidism
- B. Hyperparathyroidism (Correct Answer)
- C. Hypoparathyroidism
- D. Hyperthyroidism
Explanation: ***Hyperparathyroidism*** - This mnemonic ("**bones, stones, abdominal groans, and psychiatric overtones**") perfectly describes the classic manifestations of **hypercalcemia** due to hyperparathyroidism [1]. - **Bones** refers to bone pain from increased osteoclastic activity [1], **stones** to kidney stones [1], **abdominal groans** to GI symptoms like constipation or pancreatitis [1], and **psychiatric overtones** to neuropsychiatric symptoms like depression or confusion. *Hyperthyroidism* - Characterized by symptoms of an **overactive metabolism**, such as weight loss, heat intolerance, tremor, and tachycardia [1]. - It does not typically present with the "bones, stones, and groans" triad associated with calcium imbalances. *Hypothyroidism* - Involves symptoms of an **underactive metabolism**, including weight gain, cold intolerance, fatigue, and bradycardia. - While it can cause some psychiatric symptoms (e.g., depression), it does not involve issues like kidney stones or significant bone problems from hypercalcemia. *Hypoparathyroidism* - Leads to **hypocalcemia**, presenting with symptoms like **tetany**, muscle cramps, paresthesias, and seizures. - This is the opposite of hyperparathyroidism and would not cause the symptoms listed in the mnemonic.
Question 2: Which of the following is not a treatment option for hypercalcemia?
- A. Strontium (Correct Answer)
- B. Bisphosphonates
- C. Steroids
- D. Phosphate
Explanation: ***Strontium*** - **Strontium ranelate** is primarily used in the treatment of **osteoporosis** to promote bone formation and inhibit bone resorption. - It does not have a recognized role in the acute or long-term management of **hypercalcemia** and could potentially worsen it due to its bone-targeting effects if not carefully managed. *Steroids* - **Glucocorticoids** are effective in treating hypercalcemia associated with **granulomatous diseases** (e.g., sarcoidosis) and certain malignancies (e.g., multiple myeloma) by reducing calcitriol production or tumor burden. - They decrease intestinal calcium absorption and increase renal calcium excretion in conditions where 1,25-dihydroxyvitamin D is elevated. *Bisphosphonates* - **Bisphosphonates** (e.g., zoledronic acid, pamidronate) are potent inhibitors of **osteoclast-mediated bone resorption** and are a cornerstone in the treatment of moderate to severe hypercalcemia, especially due to malignancy. [1] - They are administered intravenously and act by inducing osteoclast apoptosis, thereby reducing the release of calcium from bone. [1] *Phosphate* - **Intravenous phosphate** can be used in severe, resistant hypercalcemia, as it promotes calcium deposition into bone and soft tissues, and forms insoluble calcium-phosphate complexes, thus lowering serum calcium. - Its use is limited due to risks of **ectopic calcification**, renal failure, and hypotension, and it is usually reserved for life-threatening situations where other treatments have failed.
Question 3: A 10-year-old boy has a fracture of the femur. Biochemical evaluation revealed a hemoglobin level of 11.5 g/dL and an erythrocyte sedimentation rate of 18 mm in the first hour. Serum calcium levels were 12.8 mg/dL, serum phosphorus levels were 2.3 mg/dL, alkaline phosphatase levels were 28 KA units, and blood urea levels were 32 mg/dL. Which of the following is the most probable diagnosis in his case?
- A. Renal rickets
- B. Hyperparathyroidism (Correct Answer)
- C. Skeletal dysplasia
- D. Nutritional rickets
Explanation: ***Hyperparathyroidism*** - The patient exhibits **hypercalcemia** (12.8 mg/dL), **hypophosphatemia** (2.3 mg/dL), and an **elevated alkaline phosphatase** (28 KA units), which are classic hallmarks of hyperparathyroidism. - The femur fracture suggests **bone demineralization** due to chronically elevated parathyroid hormone levels, leading to increased bone turnover. Primary hyperparathyroidism is indicated by significant hypercalcemia (calcium > 11.4 mg/dL) and may lead to complications like osteoporosis [2]. *Nutritional rickets* - This condition is typically characterized by **hypocalcemia** or **normal calcium** levels, **hypophosphatemia**, and an **elevated alkaline phosphatase** due to defective bone mineralization from vitamin D deficiency [1]. - The presented case has frank **hypercalcemia**, which rules out nutritional rickets. *Renal rickets* - Also known as renal osteodystrophy, this condition primarily results in **hypocalcemia**, **hyperphosphatemia** (due to impaired phosphate excretion), and **elevated alkaline phosphatase** [1]. - The patient's **normal blood urea** and **hypercalcemia** make renal rickets unlikely. *Skeletal dysplasia* - This is a broad term for genetic disorders affecting bone and cartilage development, often leading to abnormal bone shape and fractures. - While it can cause fractures, it does not typically present with the specific constellation of **hypercalcemia** and **hypophosphatemia** seen in this patient's biochemical profile.
Question 4: What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?
- A. Cinacalcet
- B. Bisphosphonates
- C. Calcium restriction
- D. Phosphate binders (Correct Answer)
Explanation: ***Phosphate binders*** - **Phosphate binders** are the initial treatment because **hyperphosphatemia** is the primary driver of secondary hyperparathyroidism in renal disease, triggering parathyroid hormone (PTH) release [1]. - They work by binding dietary phosphate in the gastrointestinal tract, preventing its absorption and thus lowering serum phosphate levels [1]. *Cinacalcet* - **Cinacalcet** is a calcimimetic that increases the sensitivity of calcium-sensing receptors on the parathyroid gland, reducing **PTH secretion** [1]. - It is often used if **phosphate binders** and **vitamin D analogs** are insufficient in controlling PTH, making it a second-line treatment [1]. *Bisphosphonates* - **Bisphosphonates** are used to treat osteoporosis by inhibiting osteoclast activity and reducing bone resorption. - They are generally contraindicated in advanced renal osteodystrophy due to concerns about adynamic bone disease and are not an initial treatment for **secondary hyperparathyroidism**. *Calcium restriction* - While restricting dietary calcium might seem intuitive, **hypocalcemia** is often a problem in renal disease due to impaired vitamin D activation [1]. - Overly restricting calcium can worsen hypocalcemia, which would further stimulate PTH release, thus it is not an initial treatment for **secondary hyperparathyroidism**.
Question 5: All are true about primary hyperparathyroidism except which of the following?
- A. Nephrolithiasis
- B. Loss of lamina dura
- C. Decreased calcium (Correct Answer)
- D. Increased alkaline phosphatase
Explanation: ***Decreased calcium*** - Primary hyperparathyroidism is characterized by **excessive parathyroid hormone (PTH)** secretion, which leads to **hypercalcemia (increased calcium levels)**, not decreased calcium [1]. - PTH's main actions are to raise serum calcium by increasing **bone resorption**, **renal calcium reabsorption**, and **calcitriol synthesis** [2]. *Nephrolithiasis* - **Hypercalcemia** from primary hyperparathyroidism leads to increased calcium excretion in the urine, increasing the risk of **calcium oxalate stones** (nephrolithiasis) [3]. *Increased alkaline phosphatase* - PTH stimulates osteoclastic activity, leading to **increased bone turnover** and release of enzymes like **alkaline phosphatase**, particularly in cases with significant bone involvement. - Alkaline phosphatase levels may also be elevated due to **osteitis fibrosa cystica**, a severe form of bone disease associated with primary hyperparathyroidism. *Loss of lamina dura* - Chronic hyperparathyroidism can cause characteristic changes in bone, including the **resorption of the lamina dura** around the teeth, which is visible on dental radiographs. - This is a direct consequence of PTH-mediated **osteoclastic activity** in areas of high bone turnover.
Question 6: A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?
- A. Active 24,25 dihydroxy cholecalciferol
- B. PTH (Correct Answer)
- C. Serum phosphate level
- D. Calcitonin
Explanation: ***PTH*** - **Parathyroid hormone (PTH)** is the primary regulator of calcium homeostasis and the key hormone that **increases in response to hypocalcemia** (low serum calcium). - In a patient on a low calcium diet for 8 weeks, **PTH secretion increases** to maintain normal serum calcium levels. - PTH acts through three main mechanisms: increasing **bone resorption** (releasing calcium from bone), enhancing renal **calcium reabsorption** in the distal tubule, and stimulating the production of **active vitamin D (1,25-dihydroxycholecalciferol)** which increases intestinal calcium absorption. *Active 24,25 dihydroxy cholecalciferol* - **24,25-dihydroxycholecalciferol** is a relatively **inactive metabolite** of vitamin D and represents a pathway of vitamin D catabolism, not activation. - The **active form** of vitamin D that increases calcium absorption is **1,25-dihydroxycholecalciferol (calcitriol)**, whose production is stimulated by PTH. - This metabolite does **not increase** in response to hypocalcemia as a compensatory mechanism. *Serum phosphate level* - A low calcium diet would **not directly lead to an increase in serum phosphate levels**. - In fact, PTH (which increases in response to low calcium) typically causes a **decrease in serum phosphate** by promoting renal phosphate excretion (phosphaturic effect). - High phosphate levels can actually exacerbate hypocalcemia by forming insoluble calcium-phosphate complexes. *Calcitonin* - **Calcitonin** is released from the thyroid parafollicular cells (C cells) in response to **high serum calcium levels** (hypercalcemia). - It acts to **lower** calcium by inhibiting osteoclast activity and reducing renal calcium reabsorption. - In hypocalcemia (low calcium diet), calcitonin secretion would **decrease, not increase**, making this the opposite of what occurs to maintain calcium homeostasis.
Question 7: A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -
- A. Scurvy
- B. Secondary Hyperparathyroidism (Correct Answer)
- C. Vitamin D Resistant rickets
- D. Primary Hyperparathyroidism
Explanation: ***Secondary Hyperparathyroidism*** - **Chronic renal failure** causes **hyperphosphatemia** and **decreased production of calcitriol (active vitamin D)**. - This leads to hypocalcemia, which stimulates the parathyroid glands to produce excessive **parathyroid hormone (PTH)**, resulting in bone demineralization and **pathological fractures** [2]. *Scurvy* - Caused by **vitamin C deficiency**, leading to impaired collagen synthesis and fragility of blood vessels. - While it can cause bone pain and potential for fractures in severe cases, it is not directly associated with **chronic renal failure** as a primary cause of pathological fracture. *Vitamin D Resistant rickets* - This is a genetic disorder (e.g., X-linked hypophosphatemia) characterized by impaired renal phosphate reabsorption and normal or elevated PTH levels. - While it causes bone demineralization, it is typically a **childhood-onset condition** [1] and not directly linked to **acquired chronic renal failure** in a 70-year-old male. *Primary Hyperparathyroidism* - Characterized by autonomous **overproduction of PTH** due to parathyroid gland adenoma or hyperplasia, leading to **hypercalcemia** and hypophosphatemia. - Unlike secondary hyperparathyroidism, which is a compensatory response to hypocalcemia in the context of renal failure, primary hyperparathyroidism is a direct parathyroid gland pathology.
Question 8: False about syphilis is :
- A. Secondary syphilis is due to hematological dissemination
- B. "General paresis of Insane" is due to CNS involvement in tertiary syphilis.
- C. Syphilitic ulcers(Chancre) are extremely painful (Correct Answer)
- D. Incubation period is 9-90 days
Explanation: ***Syphilitic ulcers (Chancre) are extremely painful*** - **Syphilitic chancres** are typically **painless** ulcers, which is a key diagnostic feature differentiating them from other genital ulcers [1]. - The absence of pain often leads individuals to delay seeking medical attention, contributing to disease progression. *Secondary syphilis is due to hematological dissemination* - **Secondary syphilis** arises from the **hematogenous (bloodstream) and lymphatic dissemination** of <i>Treponema pallidum</i> throughout the body [1]. - This widespread dissemination accounts for the **systemic symptoms** and mucocutaneous lesions observed in secondary syphilis [1]. *"General paresis of Insane" is due to CNS involvement in tertiary syphilis.* - **General paresis of the insane** (or **paretic neurosyphilis**) is a manifestation of **tertiary neurosyphilis**, resulting from chronic inflammation and atrophy of the brain parenchyma. - It leads to progressive **cognitive decline, personality changes, and neurological deficits** due to central nervous system (CNS) damage by the spirochete. *Incubation period is 9-90 days* - The **incubation period** for syphilis, from exposure to the appearance of a **chancre**, typically ranges from **9 to 90 days**, with an average of about 21 days. - This variability depends on factors such as the inoculum size and the individual's immune response.
Question 9: A 20-year-old male presents to the emergency department with a head injury. Examination reveals normal consciousness, no neurological deficits, and blood in the tympanic membrane. What is the most likely cause?
- A. Subdural haemorrhage
- B. Basilar skull fracture (Correct Answer)
- C. Intraventricular haemorrhage
- D. Extradural haemorrhage
Explanation: ***Basilar skull fracture*** - **Blood in the tympanic membrane** (hemotympanum) is a classic sign of a **basilar skull fracture**, indicating a fracture extending into the petrous part of the temporal bone. - Despite the potential severity of a basilar fracture, patients can initially present with **normal consciousness** and **no focal neurological deficits**. - Other signs of basilar skull fracture include Battle's sign (postauricular ecchymosis), raccoon eyes (periorbital ecchymosis), and CSF rhinorrhea/otorrhea. *Subdural haemorrhage* - A subdural hemorrhage is a collection of blood between the **dura mater and arachnoid mater**, typically resulting in neurological deficits due to brain compression. - While head injury is the cause, it does not directly explain **blood in the tympanic membrane** as a primary finding. *Extradural haemorrhage* - An extradural (epidural) hemorrhage is often characterized by a **lucid interval** followed by rapid neurological deterioration due to arterial bleeding. - It does not typically manifest with **blood in the tympanic membrane** unless there's a co-occurring basilar fracture, which would be the more direct cause of the tympanic finding. *Intraventricular haemorrhage* - An intraventricular hemorrhage involves bleeding into the **brain's ventricular system** and is usually associated with significant neurological impairment and altered consciousness. - It does not cause **blood in the tympanic membrane**.
Question 10: Where is a bruit typically heard in the thyroid gland?
- A. Upper pole (Correct Answer)
- B. Lower pole
- C. Middle part
- D. Lateral aspect
Explanation: **Explanation:** The presence of a thyroid bruit is a classic clinical sign of **Graves' disease** (toxic diffuse goiter). It occurs due to the hyperdynamic circulation and significantly increased vascularity of the gland. **Why the Upper Pole is Correct:** The bruit is most commonly heard over the **upper pole** of the thyroid gland. This is because the **superior thyroid artery**, a direct branch of the external carotid artery, enters the gland at the upper pole. Due to its proximity to a major high-pressure arterial trunk and its relatively superficial location, the turbulent blood flow (hypervascularity) is most audible at this site. **Analysis of Incorrect Options:** * **Lower Pole:** While the inferior thyroid artery (from the thyrocervical trunk) supplies the lower pole, it is situated deeper and has a more tortuous course, making a bruit less likely to be localized here compared to the superior pole. * **Middle Part & Lateral Aspect:** These areas represent the body of the lobes. While vascularity is increased throughout in Graves' disease, the primary inflow points (the poles) are the high-yield areas for auscultation. **High-Yield Clinical Pearls for NEET-PG:** 1. **Bruit vs. Thrill:** A bruit is an auditory sign (auscultation), whereas a **thrill** is its tactile equivalent (palpation). Both indicate Graves' disease. 2. **Differential Diagnosis:** A thyroid bruit must be distinguished from a **venous hum** (disappears with pressure over the internal jugular vein) and a **carotid bruit** (heard lateral to the gland). 3. **Significance:** The presence of a bruit is highly specific for Graves' disease and helps differentiate it from other causes of thyrotoxicosis, such as toxic multinodular goiter or thyroiditis.
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